Transmission of cml or of t(9; 22) and bcr/abl? They are not the same
Transmission of cml or of t(9; 22) and bcr/abl? They are not the same"
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Access through your institution Buy or subscribe In a recent Letter to the Editor de Brito _et al._1 describe a transplant donor retrospectively found to have t(9;22) and _BCR/ABL_ along
with other cytogenetic abnormalities often associated with acute phase or blastic transformation of CML. There are several interesting points including: (1) the donor had normal blood
parameters and no evolution to chronic or acute phase CML for >6 months (but possibly several years) when t(9;22) and _BCR/ABL_ were detected in a substantial proportion of her myeloid
cells; (2) although the donor was chimeric for cells with and without t(9;22) and _BCR/ABL_, initial engraftment was with the normal donor cells; and (3) the recipient did not develop
chronic or acute phase CML after >6 months follow-up. Several points warrant consideration. First, it was reported many years ago that persons with chronic phase CML at diagnosis may have
CML cells with cytogenetic abnormalities consistent with acute phase.2 This is conceptually consistent with recent data from ultra-deep sequencing of the _BCR/ABL_ tyrosine kinase domain in
persons with chronic phase CML, where many mutations are identified before drug exposure.3 These data suggest a long latency from acquisition of _BCR/ABL_ to diagnosis of chronic phase CML.
Second, having _BCR/ABL_ is not equivalent to having CML. Data from several centres report normal persons with _BCR/ABL_.4 The point is that to have CML the _BCR/ABL_ mutation must be in a
cell biologically capable of causing the disease. Whether this was so in this donor (and/or recipient) is unknown. Consequently, starting CML therapy may have been premature and/or
unnecessary, especially absent data-treating chronic phase CML earlier is of benefit. Third, latency from _BCR/ABL_ to developing CML is unknown and likely highly variable. The common notion
derived from the A-bomb survivors of 10–15 years latency is probably wrong. Some children with typical CML, t(9;22) and _BCR/ABL_, were diagnosed before age 1 year and have a somatic
(acquired) mutation implying CML latency can be<2 years. Also, our and other reviews of the A-bomb data suggest an early peak of CML may have occurred<5 years and even<2 years after
exposure.5 Organised surveillance of CML risk did not begin until about 10 years after the A-bomb exposures. More importantly, an increased CML-risk persisted in exposed persons for up to
40 years.6 Based on these data and the ages of donor and recipient, they may never have developed CML in their lifetimes. We do not fault de Brito _et al._ for treating these persons but it
may have been unnecessary. Certainly it would have been interesting to follow these persons to determine if they developed CML. A final point is CML cells do not always have a substantial
growth advantage over normal myeloid cells, which is often used to explain why the chronic phase CML clone eventually displaces (or replaces) normal haematopoietic cells. In this case
initial engraftment was with normal donor cells followed by appearance of cells from the CML clone but no clinical features of CML for >6 months. This is a preview of subscription
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Learn more Buy this article * Purchase on SpringerLink * Instant access to full article PDF Buy now Prices may be subject to local taxes which are calculated during checkout ADDITIONAL
ACCESS OPTIONS: * Log in * Learn about institutional subscriptions * Read our FAQs * Contact customer support REFERENCES * de Brito MD, Campilho F, Branca R, Vaz CP, Campos A . Inadvertent
transmission of occult CML through allo-SCT. _Bone Marrow Transplant_ 2015; 50: 598. Article CAS Google Scholar * Sadamori N, Matsunaga M, Yao E, Ichimaru M, Sandberg AA . Chromosomal
characteristics of chronic and blastic phases of Ph-positive chronic myeloid leukemia. _Cancer Genet Cytogenet_ 1985; 15: 17–24. Article CAS Google Scholar * Soverini S, De Benedittis C,
Machova Polakova K, Brouckova A, Horner D, Iacono M _et al_. Unraveling the complexity of tyrosine kinase inhibitor-resistant populations by ultra-deep sequencing of the BCR-ABL kinase
domain. _Blood_ 2013; 122: 1634–1648. Article CAS Google Scholar * Bose S, Deininger M, Gora-Tybor J, Goldman JM, Melo JV . The presence of typical and atypical BCR-ABL fusion genes in
leukocytes of normal individuals: biologic significance and implications for the assessment of minimal residual disease. _Blood_ 1998; 92: 3362–3367. CAS PubMed Google Scholar * Hsu WL,
Preston DL, Soda M, Sugiyama H, Funamoto S, Kodama K _et al_. The incidence of leukemia, lymphoma and multiple myeloma among atomic bomb survivors: 1950-2001. _Radiat Res_ 2013; 179:
361–382. Article CAS Google Scholar * Radivoyevitch T, Jankovic GM, Tiu RV, Saunthararajah Y, Jackson RC, Hlatky LR _et al_. Sex differences in the incidence of chronic myeloid leukemia.
_Radiat Environ Biophys_ 2014; 53: 55–63. Article Google Scholar Download references AUTHOR INFORMATION AUTHORS AND AFFILIATIONS * Division of Experimental Medicine, Department of
Medicine, Haematology Research Centre, Imperial College London, London, UK R P Gale & J F Apperley Authors * R P Gale View author publications You can also search for this author
inPubMed Google Scholar * J F Apperley View author publications You can also search for this author inPubMed Google Scholar CORRESPONDING AUTHOR Correspondence to R P Gale. ETHICS
DECLARATIONS COMPETING INTERESTS The authors declare no conflict of Interest. RIGHTS AND PERMISSIONS Reprints and permissions ABOUT THIS ARTICLE CITE THIS ARTICLE Gale, R., Apperley, J.
Transmission of CML or of t(9; 22) and _BCR/ABL_? They are not the same. _Bone Marrow Transplant_ 50, 1582 (2015). https://doi.org/10.1038/bmt.2015.199 Download citation * Published: 14
September 2015 * Issue Date: December 2015 * DOI: https://doi.org/10.1038/bmt.2015.199 SHARE THIS ARTICLE Anyone you share the following link with will be able to read this content: Get
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